eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Palatal & Maxillofacial Surgery
Snoring and Obstructive Sleep Apnea, CPAP
Updated: Oct 6, 2008
Introduction
Background
Upper airway obstruction occurring during sleep (ie, sleep-disordered breathing [SDB]) was first demonstrated in the 1960s. SDB represents a group of physiopathologic conditions that are characterized by an abnormal respiratory pattern during sleep that can be isolated or can coexist with other respiratory, nervous, cardiovascular, or endocrine diseases. Sleep-disordered breathing (SDB) is now known to be widely prevalent in the general population, and it is responsible for or contributes to numerous problems, ranging from fragmented sleep patterns to hypertension to traffic accidents.
Sleep-disordered breathing (SDB) includes obstructive sleep apnea (OSA), which consists of breathing cessations of at least 10 seconds occurring in the presence of inspiratory efforts during sleep. Central sleep apnea consists of similar apneas, but these instead take place in the absence of inspiratory efforts.
The obstructive sleep apnea syndrome (OSAS) is defined by an apnea-hypopnea index (the total number of episodes of apnea and hypopnea per hour of sleep) of 5 or higher in association with excessive daytime somnolence.
Obstructive sleep apnea syndrome (OSAS) is a potentially disabling condition characterized by excessive daytime sleepiness, disruptive snoring, repeated episodes of upper airway obstruction during sleep, and nocturnal hypoxemia.
Risk factors for sleep apnea include obesity, increased neck circumference, craniofacial abnormalities, hypothyroidism, and acromegaly. Daytime consequences include excessive sleepiness, impaired cognitive performance, and disturbed moods with a reduced quality of life. Excessive daytime sleepiness is reported to be associated with a higher risk of motor vehicle accidents and work place injuries or poor work performance .
If not adequately diagnosed and treated, obstructive sleep apnea syndrome (OSAS) is associated with severe complications such as hypertension, strokes, coronary disease, and neurobehavioral complaints and is probably a predictor of premature death. At least 50% of patients with heart failure have sleep respiratory apneas, and patients with moderate-severe obstructive sleep apnea syndrome (OSAS) have a 3-fold increased risk of developing hypertension.
In general, everyone with sleep-disordered breathing (SDB) snores, but not everyone who snores has sleep-disordered breathing (SDB). Snoring in the absence of sleep-disordered breathing (SDB) is termed primary or simple snoring. However, some evidence indicates that snoring is one end of a clinical continuum with an opposite extreme of severe obstructive sleep apnea. Some health problems may be associated even with primary snoring.
Upper airway resistance syndrome (UARS) is characterized by snoring with increased resistance in the upper airway, resulting in arousals during sleep. This can disturb sleep architecture to the point of causing daytime somnolence. No distinct diagnostic criteria exist for this entity. Patients with upper airway resistance syndrome (UARS) can be treated with nasal continuous positive airway pressure (n-CPAP).
Laryngopharyngeal reflux can cause a patient to suddenly awaken from sleep, gasping for breath. A feeling of terror is often present.
Inadequate sleep time can cause excessive daytime sleepiness. This may be involuntary, as in insomnia, or voluntary. Insomnia is characterized by the inability to fall asleep or awakening during the night and being unable to fall back to sleep. Inadequate sleep time occurs for other voluntary reasons (eg, working more than one job, family responsibilities).
Patients with hypothyroidism can also present with fatigue, daytime somnolence, and obesity. Sleep-disordered breathing (SDB) and hypothyroidism can coexist.
Narcolepsy can also cause excessive daytime sleepiness.
Pathophysiology
Any factors that decrease upper airway size or patency during sleep can lead to intermittent obstruction during inspiration, despite inspiratory effort. If the obstruction is sufficiently prolonged, blood-oxygen levels drop. Then, the patient arouses or awakens. The arousals disrupt normal sleep architecture. These, together with the oxygenation drops, are responsible for the more severe accompaniments of sleep-disordered breathing (SDB), including hypertension, arrhythmias, and death.
Factors affecting upper airway size or patency include numerous anatomic variants and abnormalities (eg, nasal obstruction, retrognathia, macroglossia), obesity, alcohol or sedative intake, and body position during sleep.
Obesity contributes to sleep-disordered breathing (SDB) by changing pharyngeal size and shape. Fat storage in the neck may be particularly associated with risk for sleep-disordered breathing (SDB), although a subset of patients with sleep-disordered breathing (SDB) are of normal body weight. Many of these patients have a family history of snoring or sleep-disordered breathing (SDB).
Alcohol intake near bedtime can cause or worsen sleep-disordered breathing (SDB) by reducing the activity of the upper airway dilating muscles. Alcohol increases both the number and duration of apneic or hypopneic events.
Frequency
United States
Sleep apnea occurs in 4% of men and 2% of women aged 30-60 years. Hypersomnolence is reported with a percentage of 16% in men and 22% in women, while 24% of men and 9% of women have an apnea-hypopnea index of at least 5.
International
Some researchers have noticed an increased incidence of OSA in persons of Asian origin.
Mortality/Morbidity
Excessive daytime sleepiness resulting from sleep-disordered breathing (SDB) can impact focus and concentration, causing decreased work effectiveness. Even mild-to-moderate sleep-disordered breathing (SDB) increases reaction time, causing performance decreases similar to alcohol intoxication. This can lead to motor vehicle accidents and other serious accidents in situations where alertness is required for safety (eg, heavy machinery operators).
Moderate-to-severe obstructive sleep apnea (OSA) is associated with earlier death. The cardiovascular sequelae of untreated obstructive sleep apnea (OSA) include hypertension, cor pulmonale, arrhythmias, and increased risk of myocardial infarction or stroke.
Recent studies have examined the relationship between OSA and glucose tolerance, and many have shown a direct and independent relationship between obstructive sleep apnea (OSA) and diabetes. The Wisconsin Sleep Study Cohort showed a greater prevalence of diabetes in subjects with increasing levels of OSA.1 Recently, several studies have shown a beneficial effect on CPAP therapy on insulin resistance or glucose levels. The probable mechanisms connecting OSA with glucose tolerance and type 2 diabetes mellitus includes the increased sympathetic activity, the sympathovagal dysfunction, alterations in neuroendocrine function (especially in GH and cortisol levels), high inflammatory state with an increase in the release of proinflammatory cytokines.Race
The prevalence of obstructive sleep apnea syndrome (OSAS) among African-American persons seems to be at least equal to and may exceed that among white persons. The prevalence among men in urban India and men and women in Korea is similar to that observed in Western countries.
Sex
All the epidemiological studies indicate that sleep apnea syndrome is more common in men than in women (the male-to-female ratio is 2-3: 1). Epidemiologic studies have reported that obstructive sleep apnea syndrome (OSAS) is a common disorder affecting about 4% of adult males and 2% of adult females.
A retrospective study on 830 patients with OSAS reports a male-to-female ratio (M:F) that increases with the gravity of the disease: 2.2:1 in mild OSAS and 7.9:1 in severe OSAS.2
The discrepancy between the lower prevalence of obstructive sleep apnea (OSA), the greater frequency of obesity, and the smaller airway size in women compared with men suggests that a gender difference underlies this condition.
Men tend to have a larger but more collapsible airway during mandibular movement than women and this, in part, may play a role in the positional dependency and severity of obstructive sleep apnea (OSA) in men.
The gender-related protective effect decreases in females who are postmenopausal and not on hormone replacement therapy.
Another possible reason of the lower prevalence of OSAS may be due to the reluctance of many women to report symptoms, mostly considered inappropriate, like snoring, causing a clinical underestimation of the problem in females.
Age
The association between age and obstructive sleep apnea is complex. Several studies have shown a higher prevalence of obstructive sleep apnea in elderly persons compared with middle-aged persons, although daytime symptoms may be less common with advancing age.
The Sleep Heart Health Study demonstrated that the influence of male sex and body mass index on obstructive sleep apnea tends to wane with age. For unclear reasons, the overall prevalence of obstructive sleep apnea plateaus after 65 years of age.
Clinical
History
The first clue in the history of patients with sleep-disordered breathing (SDB) is loud snoring. This is accompanied by breathing cessation; gasping, choking, and snorting; frequent arousals from sleep; and respiratory effort with no air. Nocturnal arrhythmias and acute blood pressure increases may occur. Morning headaches that dissipate as the day goes on, excessive daytime sleepiness, and poor concentration affect daytime performance. The disorder has been linked to an increased risk of angina, myocardial ischemia, stroke and motor vehicle crashes.
Older men may report getting up numerous times during the night to urinate and are convinced that they awaken because of the urge to urinate. The truth is often the reverse, that they awaken as a result of sleep-disordered breathing (SDB) and then they notice the urge to urinate. These patients are often surprised at their decreased need for nocturnal urination after successful sleep-disordered breathing (SDB) treatment.
Physical
Most patients with sleep-disordered breathing (SDB) are overweight or obese. A patient with a short, thick neck may be predisposed to sleep-disordered breathing (SDB). Scalloped indentations along the lateral tongue (from teeth) are a marker for relative tongue/mandibular arch size mismatch, which may predispose individuals to sleep-disordered breathing (SDB).
Causes
Important clinical risk factors for sleep-disordered breathing (SDB) are as follows:
- Nasal obstruction
- Craniofacial abnormalities
- Mandibular retrognathia
- Micrognathia
- Narrowed, tapered, and short maxillary arch
- Overbite
- Long soft palate
- Modified Mallampati grade III or IV
- Macroglossia
- Tonsillar hypertrophy
- Neck circumference more than 17 inches for men and more than 16 inches for women
- Obesity
Other problems that can contribute to or exacerbate sleep-disordered breathing (SDB) are sedative or alcohol use and poor sleep hygiene.
A very small percentage of patients with sleep-disordered breathing (SDB) have central rather than obstructive sleep apnea. Central sleep apnea can be caused by various neurologic disorders or can be idiopathic.
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| Follow-up: Snoring and Obstructive Sleep Apnea, CPAP |
| References |
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References
Young T, Blustein J, Finn L, Palta M. Sleep-disordered breathing and motor vehicle accidents in a population-based sample of employed adults. Sleep. Aug 1997;20(8):608-13. [Medline].
O'Connor C, Thornley KS, Hanly PJ. Gender differences in the polysomnographic features of obstructive sleep apnea. Am J Respir Crit Care Med. May 2000;161(5):1465-72. [Medline].
Aloia MS, Stanchina M, Arnedt JT, et al. Treatment adherence and outcomes in flexible vs standard continuous positiveairway pressure therapy. Chest. Jun 2005;127(6):2085-93. [Medline].
Babu AR, Herdegen J, Fogelfeld L, et al. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med. Feb 28 2005;165(4):447-52. [Medline].
Bachour A, Hurmerinta K, Maasilta P. Mouth closing device (chinstrap) reduces mouth leak during nasal CPAP. Sleep Med. May 2004;5(3):261-7. [Medline].
Berger G, Gilbey P, Hammel I, et al. Histopathology of the uvula and the soft palate in patients with mild, moderate, and severe obstructive sleep apnea. Laryngoscope. Feb 2002;112(2):357-63. [Medline].
Berkani M, Lofaso F, Chouaid C, et al. CPAP titration by an auto-CPAP device based on snoring detection: a clinical trial and economic considerations. Eur Respir J. Oct 1998;12(4):759-63. [Medline].
Campos-Rodriguez F, Perez-Ronchel J, Grilo-Reina A, et al. Long-term effect of continuous positive airway pressure on BP in patients with hypertension and sleep apnea. Chest. Dec 2007;132(6):1847-52. [Medline].
Caples SM, Gami AS, Somers VK. Obstructive sleep apnea. Ann Intern Med. 2005;142(3):187-97. [Medline].
Chan AS, Lee RW, Cistulli PA. Dental appliance treatment for obstructive sleep apnea. Chest. Aug 2007;132(2):693-9. [Medline].
Chervin RD, Hedger K, Dillon JE, et al. Pediatric sleep questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snoring, sleepiness, and behavioral problems. Sleep Med. Feb 1 2000;1(1):21-32. [Medline].
Ciftci TU, Ciftci B, Guven SF, et al. Effect of nasal continuous positive airway pressure in uncontrolled nocturnalasthmatic patients with obstructive sleep apnea syndrome. Respir Med. May 2005;99(5):529-34. [Medline].
Ciscar MA, Juan G, Martínez V, et al. Magnetic resonance imaging of the pharynx in OSA patients and healthy subjects. Eur Respir J. Jan 2001;17(1):79-86. [Medline].
Doherty LS, Kiely JL, Lawless G, et al. Impact of nasal continuous positive airway pressure therapy on the quality of life of bed partners of patients with obstructive sleep apnea syndrome. Chest. Dec 2003;124(6):2209-14. [Medline].
Douglas NJ. Systematic review of the efficacy of nasal CPAP. Thorax. May 1998;53(5):414-5. [Medline].
Emsellem HA, Corson WA, Rappaport BA, et al. Verification of sleep apnea using a portable sleep apnea screening device. South Med J. Jul 1990;83(7):748-52. [Medline].
Exar EN, Collop NA. The upper airway resistance syndrome. Chest. Apr 1999;115(4):1127-39. [Medline].
Findley L, Unverzagt M, Guchu R, et al. Vigilance and automobile accidents in patients with sleep apnea or narcolepsy. Chest. Sep 1995;108(3):619-24. [Medline].
Fleisher KE, Krieger AC. Current trends in the treatment of obstructive sleep apnea. J Oral Maxillofac Surg. Oct 2007;65(10):2056-68. [Medline].
Flemons WW, Tsai W. Quality of life consequences of sleep-disordered breathing. J Allergy Clin Immunol. Feb 1997;99(2):S750-6. [Medline].
Flemons WW. Clinical practice. Obstructive sleep apnea. N Engl J Med. Aug 2002;15:498-504. [Medline]. [Full Text].
Flemons WW. Clinical practice. Obstructive sleep apnea. N Engl J Med. Aug 2002;347:498-504. [Medline]. [Full Text].
Fletcher EC. Can the treatment of sleep apnea syndrome prevent the cardiovascular consequences?. Sleep. Nov 1996;19(9 Suppl):S67-70. [Medline].
Fry JM, DiPhillipo MA, Curran K, et al. Full polysomnography in the home. Sleep. Sep 15 1998;21(6):635-42. [Medline].
George CF. Diagnostic techniques in obstructive sleep apnea. Prog Cardiovasc Dis. Mar-Apr 1999;41(5):355-66. [Medline].
Grunstein RR. Sleep-related breathing disorders. 5. Nasal continuous positive airway pressure treatment for obstructive sleep apnoea. Thorax. Oct 1995;50(10):1106-13. [Medline].
Harsch IA, Schahin SP, Radespiel-Troger M, et al. Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome. Am J Respir Crit Care Med. Jan 15 2004;169(2):156-62. [Medline].
Hassaballa HA, Tulaimat A, Herdegen JJ, et al. The effect of continuous positive airway pressure on glucose control in diabetic patients with severe obstructive sleep apnea. Sleep Breath. Dec 2005;9(4):176-80. [Medline].
He J, Kryger MH, Zorick FJ, et al. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest. Jul 1988;94(1):9-14. [Medline].
Hoy CJ, Vennelle M, Kingshott RN, et al. Can intensive support improve continuous positive airway pressure use in patients with the sleep apnea/hypopnea syndrome?. Am J Respir Crit Care Med. Apr 1999;159(4 Pt 1):1096-100. [Medline].
Hudgel DW, Hendricks C, Hamilton HB. Characteristics of the upper airway pressure-flow relationship during sleep. J Appl Physiol. May 1988;64(5):1930-5. [Medline].
Ip M, Mokleshi B. Sleep and glucose intolerance/diabetesmellitus. Sleep Med Clin. 2007;2:19—29.
Jean Wiese H, Boethel C, Phillips B, et al. CPAP compliance: video education may help!. Sleep Med. Mar 2005;6(2):171-4. [Medline].
Jordan AS, McEvoy RD. Gender differences in sleep apnea: epidemiology, clinical presentation and pathogenic mechanisms. Sleep Med Rev. 2003;7(5):373-6. [Medline].
Jordan AS, McEvoy RD. Gender differences in sleep apnea: epidemiology, clinical presentation and pathogenic mechanisms. Sleep Med Rev. 2003;7(5):373-6. [Medline].
Kawahara S, Akashiba T, Akahoshi T, et al. Nasal CPAP improves the quality of life and lessens the depressive symptoms in patients with obstructive sleep apnea syndrome. Intern Med. May 2005;44(5):422-7. [Medline].
Lankford DA, Proctor CD, Richard R. Continuous positive airway pressure (CPAP) changes in bariatric surgery patients undergoing rapid weight loss. Obes Surg. Mar 2005;15(3):336-41. [Medline].
Lévy P, Pepin JL. Auto-CPAP: an effective and low-cost procedure in the management of OSAS?. Eur Respir J. Oct 1998;12(4):753-5. [Medline].
Marshall NS, Neill AM, Campbell AJ, Sheppard DS. Randomised controlled crossover trial of humidified continuous positive airway pressure in mild obstructive sleep apnoea. Thorax. May 2005;60(5):427-32. [Medline].
McArdle N, Devereux G, Heidarnejad H, et al. Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med. Apr 1999;159(4 Pt 1):1108-14. [Medline].
McEachern RC, Patel RG. Pneumopericardium associated with face-mask continuous positive airway pressure. Chest. Nov 5 1997;112(5):1441-3. [Medline].
Misiolek M, Marek B, Namyslowski G, et al. Sleep apnea syndrome and snoring in patients with hypothyroidism with relation to overweight. J Physiol Pharmacol. Mar 2007;58 Suppl 1:77-85. [Medline].
Mohsenin V. Effects of gender on upper airway collapsibility and severity of obstructive sleep apnea. Sleep Med. Nov 2003;4(6):523-9. [Medline].
Morgenthaler TI, Aurora RN, Brown T, et al. Practice parameters for the use of autotitrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome: an update for 2007. An American Academy of Sleep Medicine report. Sleep. Jan 1 2008;31(1):141-7. [Medline].
Moyer CA, Sonnad SS, Garetz SL, et al. Quality of life inobstructive sleep apnea: a systematic review of the literature. Sleep Med. 2001;2:477-91. [Medline]. [Full Text].
Namyslowski G, Scierski W, Zembala-Nozynska E, et al. [Histopathologic changes of the soft palate in snoring and obstructive sleep apnea syndrome patients]. Otolaryngol Pol. 2005;59(1):13-9. [Medline].
Neill AM, Wai HS, Bannan SP, et al. Humidified nasal continuous positive airway pressure in obstructive sleep apnoea. Eur Respir J. Aug 2003;22(2):258-62. [Medline].
Netzer NC, Stoohs RA, Netzer CM, et al. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131:485-91. [Medline].
Ohayon MM, Guilleminault C, Priest RG, et al. Snoring and breathing pauses during sleep: telephone interview survey of a United Kingdom population sample. BMJ. Mar 22 1997;314(7084):860-3. [Medline].
Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. Dec 20 2000;284(23):3015-21. [Medline].
Reichmuth KJ, Austin D, Skatrud JB, et al. Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med. Dec 15 2005;172(12):1590-5. [Medline].
Remmers JE, DeGroot WJ, Sauerland EK, et al. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol: Respirat Environ Exercise Physiol. 1978;44:931–938. [Medline].
Roth T, Zammit G, Kushida C, et al. A new questionnaire to detect sleep disorders. Sleep Med. 2002;3(2):99-108. [Medline].
Sadikot SM. An overview: Obstructive Sleep Apnea and the Metabolic Syndrome: Should ‘‘X'' be changed to ‘‘Zzz. . . zzzz. . . . Zzzz zzzzz. . . .Zzz''?. Diabetes & Metabolic Syndrome. 2007;1:287—302.
Saletu M, Sauter C, Lalouschek W, et al. Is excessive daytime sleepiness a predictor of carotid atherosclerosis in sleep apnea?. Atherosclerosis. Feb 2008;196(2):810-6. [Medline].
Saunamäki T, Jehkonen M. A review of executive functions in obstructive sleep apnea syndrome. Acta Neurol Scand. Jan 2007;115(1):1-11. [Medline]. [Full Text].
Schwartz DJ, Kohler WC, Karatinos G. Symptoms of depression in individuals with obstructive sleep apnea may be amenable to treatment with continuous positive airway pressure. Chest. Sep 2005;128(3):1304-9. [Medline].
Series F. Evaluation of treatment efficacy in sleep apnea hypopnea syndrome. Sleep. Nov 1996;19(9 Suppl):S71-6. [Medline].
Souter MA, Stevenson S, Sparks B, et al. Upper airway surgery benefits patients with obstructive sleep apnoea who cannot tolerate nasal continuous positive airway pressure. J Laryngol Otol. Apr 2004;118(4):270-4. [Medline].
Stammnitz A, Jerrentrup A, Penzel T, et al. Automatic CPAP titration with different self-setting devices in patients with obstructive sleep apnoea. Eur Respir J. Aug 2004;24(2):273-8. [Medline].
Stoohs R, Guilleminault C. MESAM 4: an ambulatory device for the detection of patients at risk for obstructive sleep apnea syndrome (OSAS). Chest. May 1992;101(5):1221-7. [Medline].
Stradling JR, Hardinge M, Smith DM. A novel, simplified approach to starting nasal CPAP therapy in OSA. Respir Med. Feb 2004;98(2):155-8. [Medline].
Stradling JR, Smith D, Crosby J. Post-CPAP sleepiness--a specific syndrome?. J Sleep Res. Dec 2007;16(4):436-8. [Medline].
Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. Cooperative Group Burgos-Santander. N Engl J Med. Mar 18 1999;340(11):847-51. [Medline].
Teschler H, Berthon-Jones M. Intelligent CPAP systems: clinical experience. Thorax. Oct 1998;53 Suppl 3:S49-54. [Medline].
Thakkar K, Yao M. Diagnostic studies in obstructive sleep apnea. Otolaryngol Clin North Am. 2007;40(4):785-805. [Medline].
Victor LD. Treatment of obstructive sleep apnea in primary care. Am Fam Physician. Feb 1 2004;69(3):561-8. [Medline].
Weaver TE, Kribbs NB, Pack AI, et al. Night-to-night variability in CPAP use over the first three months of treatment. Sleep. Apr 1997;20(4):278-83. [Medline].
White DP, Gibb TJ, Wall JM, et al. Assessment of accuracy and analysis time of a novel device to monitor sleep and breathing in the home. Sleep. Feb 1995;18(2):115-26. [Medline].
Wolf J, Lewicka J, Narkiewicz K. Obstructive sleep apnea: an update on mechanismsand cardiovascular consequences. Nutr Metab Cardiovasc Dis. 2007;17:233-40. [Medline].
Young T, Shahar E, Nieto FJ, et al. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med. 2002;162(8):893-900. [Medline].
Further Reading
Keywords
CPAP, apnea, sleep apnea, snoring, obstructive sleep apnea, sleep apnea snoring, obstructive sleep apnea syndrome, OSAS, upper airway obstruction occurring during sleep, sleep-disordered breathing, SDB, upper airway resistance syndrome, UARS, laryngopharyngeal reflux, insomnia, daytime somnolence, narcolepsy, nasal continuous positive airway pressure, n-CPAP, CPAP machine, CPAP machines, CPAP masks, CPAP mask, CPAP apnea, CPAP sleep, sleep apnea treatment, sleep, snore, sleep apnea machine, apnea treatment, sleep disorder
